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This study explores the contribution of yoga as a patient choice within a continuing cardiac rehabilitation (CR) programme by comparing a group of individuals who chose to undertake a yoga programme as part of their continuing CR with a group who chose to follow a gymnasium based exercise programme. The study aims were to describe the characteristics of individuals who chose yoga (n=25) or exercise (n=35) CR programmes and explore over one year their process of adaptation and change together with the perceived benefits from the interventions. The design of this study was that of an Exploratory Between Methods Triangulation. The methods utilised were self-reports using standardized instruments including Self Perception Profile (Messer & Harter 1986), Self Evaluation of Individual Quality of Life (O'Boyle et aI, 1993) and Perceived Stress (Cohen, 1983). Semi-structured interviews captured accounts from a purposeful sample of participants at commencement of the intervention and at the end of one year. The questionnaire data was triangulated with the data and narrative from the interviews to compare the experiences, processes and any benefits achieved by participants in both the exercise and yoga groups. The key findings from this study were that the majority of yoga group participants reported that they achieved mind/body benefits including enhanced self-awareness, reduction in stress and anxiety, greater calmness, positive feelings, flexibility and suppleness within the body. The exercise group participants reported benefits of enhanced physical fitness and feelings of general well being. However, this group noted a more limited number of self-changes, which tended to be less personal and related largely to the physical dimension of their experience on the exercise programme. The findings of this study have implications for the policy and practice surrounding the future development of Cardiac Rehabilitation Programmes in relation to the nature of interventions included within such programmes and their potential to support and empower lifestyle change.

Skeletal muscle adapts to the stress of contractile activity with a change in gene expression to yield a family of highly conserved cytoprotective proteins known as heat shock proteins (HSPs). These proteins function to restore cellular homeostasis and to protect the cell against further insults. The exercise-induced stress response of rodent muscle is now relatively well defined. Comparable data from human studies, however, are extremely limited and the stress response of human skeletal muscle is far from understood. The main aims of this thesis were to characterise the time-course and magnitude of response of the exercise-induced production of the major HSP families in human skeletal muscle. The role of increased muscle and core temperature in contributing to the exercise-induced production of HSPs was also investigated. Finally, the effects of training status on baseline muscle content of the major HSP families and on the magnitude of the exercise-induced stress response was also examined. All of the exercise related studies undertaken in this thesis employed a 45 min running exercise protocol on a motorised treadmill at an intensity corresponding to the lactate threshold. This protocol was characterised as `non-damaging' in nature as it resulted in no overt structural or functional damage to the muscle of young untrained (27 ±5 years), recreationally active (25 ±2 years) or aerobically trained male subjects (27 ±6 years), as evidenced by indirect indicators of muscle damage such as circulating levels of creatine kinase and maximal quadriceps isometric muscle force. The time-course and magnitude of the exercise-induced response of the major HSP families were characterised in an active young (24 ±4 years) male population. Muscle biopsies were obtained from the vastus lateralis muscle immediately prior to and at 24 h, 48 h, 72 h and 7 days post-exercise. Exercise induced significant and individually variable increases in HSP70, HSC70 and HSP60 content with peak increases typically occurring at 48 h post-exercise. In contrast, exercise did not induce significant increases in either HSP27, aB-crystallin, manganese superoxide dismutase (MnSOD) protein content or the activity of superoxide dismutase (SOD) and catalase. When examining baseline protein levels, HSC70, HSP27 and aB-crystallin appeared consistently expressed between subjects whereas HSP70 and MnSOD displayed marked individual variation of up to 3 and 1.5 fold, respectively. These data demonstrate a differential effect of aerobic exercise on specific HSPs. Data also demonstrate an individual variation in both basal HSP levels and in the magnitude of the stress response to acute exercise, which may be related to individual differences in training status. The role of increased muscle and core temperature in contributing to the exercise induced production of HSPs were subsequently investigated. Active young males (23 A: 3 years) underwent a passive heating protocol of 1h duration during which the temperature of the core and vastus lateralis muscle were increased to similar levels as that occurring during exercise. One limb was immersed in a tank containing warm water whilst the contra-lateral limb remained outside the tank and was not exposed to heat stress. Muscle biopsies were obtained from the vastus lateralis of both legs immediately prior to and at 48 h and 7 days post-heating. The heating protocol induced significant increases in rectal and muscle temperature of the heated leg whilst muscle temperature of the non-heated limb showed no significant change following heating. The heating protocol failed to induce significant increases in muscle content of HSP70, HSC70, HSP60, HSP27, aB-crystallin, MnSOD protein content or the activity of SOD and catalase in either the heated or non-heated leg. Data demonstrate that increases in both systemic and local muscle temperature per se appear not to be mediating the exercise-induced production of HSPs and suggest that non-heat-stress factors associated with muscle contractile activity are of more importance in mediating this response. The influences of aerobic training status on the basal levels of HSPs and on the magnitude of the exercise-induced stress response were also investigated. Muscle biopsies were obtained from the vastus lateralis of young trained (28 ±6 years) and untrained (29 ±6 years) male subjects immediately prior to and at 48 h and 7 days post-exercise. When comparing muscles at rest, trained subjects had significantly higher levels of aB-crystallin, HSP60 and MnSOD compared with untrained subjects. Trained subjects also had a tendency for higher levels of HSP70, HSC70 and total SOD activity compared with untrained subjects. In contrast to the active population examined earlier, neither the trained nor untrained subjects exhibited a stress response to exercise. The absence of a stress response in trained subjects is likely due to the increase in baseline defences and the customary nature of the exercise protocol. The absence of a stress response in untrained subjects may be due to the failure of the exercise protocol to elicit a proposed critical threshold intensity that is required to induce increases in muscle HSP content. This thesis has provided novel data for the literature and has significantly advanced our understanding of the exercise-induced stress response of human skeletal muscle. Future research should examine the effects of exercise intensity on muscle HSP production and investigate the role of reactive oxygen species in contributing to the response. The wider implications of the exercise-induced production of HSPs, such as their potential cytoprotective properties against related and non-related stressors, should also be examined.

Approximately 3.6 million individuals in the UK are involved in a type of shift-work which impinges on the normal nocturnal sleeping period. This prevalence has significance considering that shift-work is a risk factor for many health problems including cardiovascular disease, breast cancer, metabolic syndrome, obesity and gastrointestinal symptoms (e.g., constipation). These health inequalities are generally under-researched. Past studies have also focused on chrono-biological related reasons (e.g., exposure to light at night) rather than lifestyle factors. Physical activity is reported to be beneficial for many aspects of day-worker's health. However, there is a dearth of knowledge regarding the relationship between physical activity, adiposity and gastrointestinal symptoms in shift-workers. Thus, the aim of this thesis was to explore, using a multidisciplinary approach, the relationships between body mass index (8M I), appetite regulation, gastrointestinal health and physical activity during shift-work and night-work. In the first study (presented in Chapter 3), a cross-sectional study design was adopted to explore the relationships between 8MI, gastrointestinal symptoms and leisure-time physical activity (LTPA) in shift-workers. The data from this study indicated that the least active shift-workers had the highest mean 8MI, 73% of these workers being overweight or obese. Nevertheless, dose-response effects of LTPA on 8MI were not evident. A positive relationship was present between physical activity level and frequency of heartburn but not other digestive symptoms (e.g., diarrhoea). In the studies presented in Chapters 4 and 5, the effects of an acute bout of evening exercise upon appetite-related factors were investigated during a simulated night-shift. In Chapter 4, the protocol was characterised by a feeding schedule typically adopted by many shift-workers, Le. eating smaller but more frequent portions of food rather than one large meal. In contrast, the protocol in Chapter 5 was characterised by a feeding schedule designed to be more in line with what day-workers do during their work-period, i.e. eating one larger meal 3-4 h after the work period has started. Findings from Chapter 4 indicate that, unlike after diurnal exercise, circulating concentrations of acylated ghrelin and leptin during a night-shift are increased by prior evening exercise. However, hunger during the night-shift was unaffected by prior evening exercise in this study. In the subsequent experiment involving one large meal, nocturnal concentration of serum leptin was increased by exercise but there was little effect on plasma acylated ghrelin level. Again, night-shift hunger was unaffected by prior evening exercise. Taken together, these findings indicated that exercise mediates different effects on appetite-related hormones at night and that meal frequency is an important factor which regulates the response of acylated ghrelin, but not leptin. Despite the above findings, mean night-shift hunger was unaffected by evening exercise, regardless of meal frequency. This implies that a compensatory increase in food intake during the night-shift in response to prior exercise may not occur, thus supporting the notion that exercise can mediate a negative energy balance which might attenuate body mass gain in shift-workers. The study presented in Chapter 6 determined the within-subject correlations between factors that regulate appetite in the post-exercise period. This study explored how circulating levels of acylated ghrelin and leptin are controlled at night following evening exercise. The findings from Chapter 6 suggested that exercise related changes in plasma acylated ghrelin concentration are negatively correlated to those in circulating levels of glucose and insulin, but not those in non-esterified fatty acids (NEFA) or triglyceride. The aforementioned Significant correlations were not reported in daytime studies. Post-exercise alterations in serum leptin level were also found to be related to those in circulating levels of insulin but not those in glucose, NEFA or triglyceride. The exercise-related alterations in circulating level of acylated ghrelin, but not leptin were correlated with the changes in hunger during the post-exercise period throughout the night. In the study presented in Chapter 7, a randomised controlled trial was employed to examine the effect of altering (via motivational interviewing over a three month period) a shift-worker's physical activity and dietary habits on their adiposity and gastrointestinal symptoms. The findings presented in Chapter 7 indicate that a 12-week motivational interviewing intervention which focused upon increasing physical activity level and improving dietary habits significantly attenuated an increase in 8MI, but not waist-to-hip ratio or frequency of digestive symptoms in UK shift-workers. In summary, this thesis makes a significant contribution to the field of physical activity and shift-work. This thesis demonstrates that relationships between 8MI, appetite regulation, gastrointestinal health (l.e., heartburn) and physical activity do exist during shift-work and night-work.

Injuries in professional soccer are common with the financial cost running into many millions of pounds. The incidence of re-injury on return to competitive action accounts for a high proportion of all injuries with inadequate rehabilitation being identified as one of the major factors when considering re-injury. Methods of improving the rehabilitation outcomes could therefore reduce the overall incidence of injury and may improve team performance through greater player availability. The accuracy of the available literature addressing the epidemiology of soccer injuries is questionable. It was therefore necessary to establish the incidence of soccer injury and reinjury using comprehensive data collection methods. A data collection method based on the principals of first hand injury observation, comprehensive and immediate recording of injuries and accurately timed exposure for both training and competitive matches was therefore designed. Study 1 used these methods to scrutinise the results of previously published literature. Results showed that the definition of the term 'injury' can have a significant effect on the results from epidemiological studies of soccer injuries. It was also observed that estimating exposure can result in an under-calculation of the injury frequency rate when reporting the rate as new injuries per 1000 training or playing exposure hours. The new methods for collecting epidemiological data clearly showed that methodology is important in generating study results and was adopted for the current thesis. The data collected to evaluate approaches to data collection indicated that injury is the major cause of absence in professional soccer although this assumption had never been investigated. Study 2 evaluated this supposition by investigating what percentage of total absences soccer injuries were responsible for. The data showed that injury was the major reason for absence with 50% of the incidents of match absence and 65% of training absence being as a result of soccer related injury. Other reasons for absence were also noted. For example, sickness and suspension were areas where it was suggested that availability could be positively affected by reducing the incidence of absence as a result of these two factors. To highlight the aetiology and severity of soccer injuries at one professional soccer club, a five-season comprehensive epidemiological study was undertaken. Study 3 showed that the average percentage of the playing squad per season sustaining an injury that resulted in more than one days absence from training or playing was 86%. Over the five seasons, an average of 41% of players sustained >1 injury in any one season the severity of which resulted in more than one days absence. Eighty five percent of all injuries throughout the study period were sustained to the lower limb. When analysing both severity and anatomical location of injury, it was found that, during the 5 competitive-season period, 82 injuries were sustained to the lower limbs which resulted in an absence of >14 days. It was suggested that these injuries may necessitate alterations to habitual training patterns which may, in turn, result in detraining. This detraining may result in players returning to competition ill-prepared for the physical and physiological demands of soccer play at the elite level and increase their susceptibility to re-injury. In order that the effects of injury-induced absence could be investigated, changes in players' performance, using a battery of soccer-specific field tests, was investigated in Study 4. All players absent for >2 d through injury were tested on their return to normal squad training. These results were compared with a data set collected when the players were fit and playing competitive soccer. No significant differences were observed in any performance variables for those players absent for <14 d. The results for players absent for >14d showed no significant differences in tests to evaluate flying 20 m sprint speed, counter-movement jump height and hamstring flexibility. Significant decreases in performance were however, found in estimated V̇ O₂max, and repeated sprint ability (RSA) performance. It was suggested that the decrements in aerobic power and repeated sprint ability may be related with high aerobic power being recognised as a requirement for recovery between bouts of high-intensity exercise. It was also suggested that one of the reasons for the performance decrements may be the changes in habitual soccer training patterns during rehabilitation. To investigate this hypothesis, study 5 compared the rehabilitation training load and the training load when participating in normal squad training and playing competitive matches. A 17-month investigation to quantify and compare the two modes of training was undertaken. Players who were absent for >14 d due to soccer injury had their rehabilitation training quantified using a number of established methods. On their return to normal squad training, the same methods were used to quantify training for a period similar to the duration of their rehabilitation programme. The period of rehabilitation when players were unable to run, due to the restrictive nature of their particular pathology, lacked the intensity of exercise normally associated with squad training and playing matches. A comparison of other phases of rehabilitation and normal training found no significant differences in average heart rate or ratings of perceived exertion measures. It was therefore demonstrated that the major difference between the two training periods was during early rehabilitation. In response to the findings of Study 5, Study 6 investigated the effect of increasing the intensity of exercise during early rehabilitation in reducing the effects of detraining following injury. This final study in the thesis investigated the effects of work-matched, constant pace, continuous exercise and intermittent-paced exercise in maintaining aerobic power and RSA performance. Players injured for >14 d (n=16) were randomly allocated to one of the two intervention groups and performed either continuous or intermittent exercise on rowers, cross trainers and cycle ergometers during the period of rehabilitation that they were unable to perform running exercise. Reductions in estimated V̇ O₂max and RSA were observed in both intervention groups with the reductions in performance of the constant-pace group greater than those observed in the intermittent pace group. None of these differences however, reached significance leading to the conclusion that both intervention programmes were effective in preventing performance decrements in V̇ O₂max and one was not superior to the other. The only negative changes observed were in RSA performance decrement for both groups from pre-injury to post-injury tests. Although these changes were found to be significant, the level of change was not sufficiently great to surpass the figure calculated as the smallest meaningful change. This was due to the lack of reliability of this particular test.

With the increase in the prevalence of anabolic steroid (AS) use for non-medical performance and image enhancement purposes, the impact of AS on cardiovascular health is an issue of growing public concern. AS use has long been associated with a number of negative CV outcomes such as acute myocardial infarction, stroke, thrombo-embolisms and sudden death. These associations, however, are largely assumed from case study findings where no cause and effect can be apportioned. Small cohort studies have suggested a negative effect of AS on a number of established CV disease risk factors including, blood pressure (BP), lipid profiles (e.g total cholesterol, LDL and HDL), C-reactive proteins and homocysteine, although data is limited both in number of studies and number of participants and is often contradictory. Another potential mechanism to link AS use to cardiac events has been to assess cardiac structure and function. Available data is contradictory but recent developments in imaging technologies suggest that new mechanistic insights could be developed and/or tested. In study one we investigated the impact of AS use on a broad profile of CV risk factors as well as an in-depth cardiac assessment utilising speckle tracking echocardiography which can assess regional and global cardiac deformation in multiple planes. In AS users we observed an increase in resting heart rate and low- density lipoprotein concomitant to a decrease in high-density lipoprotein levels. 2D and speckle-tracking echocardiography revealed a significant effect of AS use on cardiac function, most notably a decreased diastolic (relaxation) function that suggests a stiffer left ventricle in the AS users. This imposes a greater workload on the heart and increases the risk of CV events. In study two we developed the assessment of cardiac structural assessment in AS users by adopting state-of-the-art magnetic resonance imaging that provides a greater accuracy in morphology assessment as well as allowing us to determine the presence of perfusion defects and interstitial fibrosis. We observed that AS users had a hypertrophy of both the left and right ventricles that was concomitant with diastolic dysfunction in the left ventricle and a reduction in right ventricular contractility. Despite these findings no AS user presented with any perfusion defect or evidence of interstitial fibrosis, suggesting that these pathways to CV events were not apparent in the current group of AS users. The final study comprised two pilot or feasibility studies of the impact of resistance exercise on left ventricular function in AS users. Trial 1 assessed blood pressure and cardiac tissue velocities during an acute leg press with and without valsalva. Systolic blood pressure was significantly elevated even after one repetition and this was mediated by AS use. In trial 2 cardiac function and blood biomarkers of cardiac cell damage were assessed before and after a standard resistance exercise training session. Left ventricular systolic function was maintained in recovery in both AS and NAS participants. Diastolic function was reduced in both groups with some evidence that AS use exaggerated this effect. Multiple technical, design and participant lessons were gained to take these feasibility studies forward to full studies. Overall we add new data to the concept that AS use can place the participant at an increased CV risk. It is probably not obligatory that AS use leads to increased CV risk but in some the route from AS use to CV event may be mediated by changes in structure and function of both the L V and RV. Exercise stress may add an additional CV risk to the AS user.

The female reproductive hormone oestrogen influences cardiovascular and thermoregulatory control. A dramatic decline in oestrogen during the menopause causes cardiovascular and thermoregulatory dysfunction resulting in hot flushes (HFs). HFs consist of feelings of intense heat with rapid increases in cutaneous vasodilation and sweating that severely affect quality of life and increase cardiovascular disease risk. Treatment using hormone replacement therapy for HFs is contraindicated in some symptomatic females meaning an alternative strategy is warranted. Exercise training may reduce HFs; however no study to date has examined the physiological mechanisms that cause changes in the frequency and severity of HFs following a period of exercise training. Exercise training is known to enhance thermoregulatory efficiency via an earlier core temperature onset for cutaneous vasodilation and sweating in pre-menopausal females. Exercise training is also known to positively impact vascular function in the conduit, cutaneous and cerebral vessels and thus can also decrease cardiovascular risk in symptomatic post-menopausal females. Heat acclimation interventions target the same thermoregulatory and cardiovascular physiological mechanisms, and may also be beneficial. The primary aim of this thesis was to (i) examine whether exercise training reduces objectively measured HFs via improving cardiovascular and thermoregulatory dysfunction in symptomatic post-menopausal females, and to (ii) assess the efficacy of an exercise-independent stimulus in improving thermoregulatory and cardiovascular function in pre-menopausal females. Twenty-one symptomatic post-menopausal females completed a 16-week exercise training intervention (n=14, 52±4y, 29±6 kg/m2) or a no-exercise control intervention (n=7, 52±6y, 30±7 kg/m2). Cardiorespiratory fitness (VO2peak) and brachial artery endothelial function was assessed using flow-mediated dilation (FMD). Participants underwent a passive heat stress in a water-perfused suit (~48ºC) to obtain core temperature thresholds and sensitivities for cutaneous vascular conductance (CVC) and sweat rate at two sites (chest and forearm). Middle cerebral artery velocity (MCAv) was measured at rest and throughout the heat stress. All measurements were repeated following the intervention period. HFs reduced by 39 HF•wk (95% CI= 31, 47) following exercise training compared to no change in control. HF-severity reduced by 101 (AU) (95% CI= 80, 121) following exercise training compared to no change in control. VO2peak and FMD improved (P<0.05), along with a lower core temperature following exercise training [0.14ºC (95% CI=0.03, 0.20; P=0.04)]. Sweat rate and CVC body/core temperature thresholds occurred ~0.22ºC earlier alongside an increase in sweating sensitivity, at both sites, following exercise training. Resting MCAv was 3.12 cm/s (95% CI, 1.20, 5.01; P=0.03) higher, with decreases in MCAv attenuated during heat stress, following exercise training. HFs recorded in symptomatic females during the passive heat stress prior to and following the exercise training (n=9) or no-exercise control (n=6) intervention were used to assess changes in thermoregulatory and (cerebro)vascular responses during an acute HF. HFs were objectively identified and divided into eight equal segments, with each segment representing 12.5% of HF duration, for analysis. Exercise training decreased HF duration by 63s (95% CI, 14, 113; P=0.08) compared to a negligible decrease of 17s (95% CI, -43, 66) following control. Chest sweat rate decreased by 0.04 mg•cm2•min-1 (95% CI, 0.02, 0.06; P=0.01) during HFs after exercise training compared to no change in control (P>0.05). This was accompanied by a reduction in chest skin blood flow of 26 AU (95% CI, 21, 30; P=0.01) during HFs following exercise training compared to no change in control (P=0.10). MCAv was attenuated by 3.4 cm/s (95% CI, 0.7, 5.1; P<0.001) during a HF following exercise training compared to control [0.6 cm/s (95% CI, -0.7, 1.8; P=0.93)].Eighteen pre-menopausal females (25±8y) were assigned to 3x30-min of cycling exercise (70% HRmax) or warm water immersion (42ºC) to the level of the sternum for 8-weeks. FMD (P=0.003) and VO2peak (P<0.001) improved following both interventions. Core body temperature reduced by 0.14ºC (95% CI, 0.04, 0.23; P=0.004) following both interventions. Sweat rate mean body temperature thresholds at the chest and forearm occurred 0.10ºC (95% CI=-0.14, 0.33, P<0.001) and 0.19ºC (0.12, 0.23ºC, P<0.001) earlier following the interventions, alongside an increase in sweat rate sensitivity of 1.18 mg•cm2•min-1 (95% CI= 0.68, 1.67; P<0.001) following water immersion compared to 0.28 mg•cm2•min-1 (95% CI= 0.23, 0.78) following exercise training. CVC core temperature thresholds occurred ~0.20ºC earlier at the chest and forearm (P<0.001). Resting MCAv was 2.30 cm/s (95% CI=1.20, 3.34; P<0.001) higher, with decreases in MCAv attenuated during heat stress, following both interventions. The findings from this thesis suggest that reductions in the frequency and severity of HFs with exercise training are mediated by improvements in thermoregulatory function, alongside cerebral, conduit and cutaneous adaptation. This coincided with objective reductions in HF severity following exercise training, with attenuation in the physiological perturbations observed during an acute HF. Consequently, interventions that target thermoregulatory function may be useful in reducing post-menopausal HFs. In keeping with the exercise mediated physiological changes, warm water immersion training also elicits similar favourable thermoregulatory, conduit- and cerebrovascular adaptations to a period of moderate intensity exercise training in pre-menopausal females. Immersion therapy may therefore be applicable to HF-symptomatic post-menopausal females.

Phenotyping of human muscle based on its profile of myosin heavy chain isoforms is commonly used to help understand changes in muscle function. However, in many instances, measureable changes in force output or contractility occur in the absence of any change in myosin heavy chain profile. Therefore, more sophisticated analysis is required. Proteomic techniques including 2-dimensional gel electrophoresis, high- performance liquid chromatography and peptide mass spectrometry can be used to investigate changes in the abundance of hundreds of proteins simultaneously. To date, such techniques have not been used to specifically characterise the human myofibrillar proteome, or study how the myofibrillar proteome relates to muscle outputs such as peak isometric force or the velocity of contraction. This thesis presents a series of studies that develop proteomic techniques for the analysis of myofibrillar proteins as well as optimisation of techniques for measuring the range of muscle output from isometric through to velocity maximum of the human knee extensor muscles in vivo. After optimisation, the proteomic and muscle function measurement were employed to study diurnal variation. Time-of-day differences in sports performance and muscle function are widely reported, and typically, performance is ~10 % greater in the evening compared to the morning. This is consistent with our result in Chapter 3; we investigated this chapter by conducting a battery of muscle performance tests in a population of well-familiarised participants. Our data show that RFD exhibits the greatest diurnal variation (18 %) followed by isometric force (10.2 %). The diurnal variation in IKD data was less robust (range 8.1 - 9.8 %), which may have been due to the lesser precision of this technique compared to MVC and RFD. Therefore MVC and RFD were used in the final study. In final study, this thesis reports significantly (P<0.05) greater peak isometric force (11 %) and rate of force development (16 %) of knee extensor muscles of young strength-trained males in the evening compared to morning. Proteomic analysis of biopsy samples of the vastus lateralis profiled more than 100 myofibrillar protein species and detected 8 significant differences in protein abundance between morning and evening samples. The greatest difference was in the abundance of the slow isoform of myosin binding protein C (MyBPC1), which is known to modulate the activity of actin-bound myosin ATPases. MyBPC1 was resolved to 6 species; therefore the difference in abundance of one species reported here likely represents a change in post-translational modification. Therefore, this thesis provides associational evidence that post-translational modification of MyBPC1 contributes to the diurnal variation in muscle function.

The aim of this thesis was to examine the influence of high-anxiety, training and expertise-level on perceptual-cognitive skills in the sport of badminton. First, the coupling between observed badminton serves, visual search behaviour and anticipation judgements of athletes ranging in expertise was investigated. Expert players produced more accurate anticipation judgements compared to novice athletes. Experts fixated vision upon body areas containing the discriminating kinematic information between serve- types more frequently and for a longer duration compared to novice players. A subsequent case-study highlighted the relationship between expertise, visual search and anticipation judgement extended to a world-class athlete. Second, the role of skill level in mediating the effects of high anxiety on anticipation and the capacity to allocate attentional resources to a secondary task was examined through high- and low-anxiety conditions. Skilled players made more accurate anticipation judgements compared to their novice counterparts, regardless of anxiety conditions. High-anxiety resulted in a decrease in secondary task performance for the novice, but not the skilled group, when compared to low-anxiety. Finding demonstrates that skilled athletes can effectively allocate attentional resources during performance, leading to the effects of anxiety being negated, whereas novices cannot. Third, a perceptual-cognitive intervention consisting of simulation training under high-anxiety conditions led to greater anticipation performance under high-anxiety and field-based conditions compared to pre-test and training under low-anxiety conditions. Overall, expert athletes make superior anticipation judgements due to different visual search behaviours and attentional resources, all of which are robust to high anxiety, when compared to lesser-skilled players, with these abilities being trainable.

Inhaled short acting β2–agonists are commonly used in the treatment of asthma, exercise induced bronchoconstriction (EIB) and airway hyperresponsiveness (AHR). The World Anti-doping Agency (WADA) permits asthmatic athletes to use inhaled salbutamol with an accumulated dosage not exceeding 1600 µg over a 24-hour period. A key driver for the inclusion of β2-agonists on the WADA restricted list is associated with its potential impact on athletic performance according to previous research. However, the findings from previous studies are equivocal and focus almost exclusively on endurance performance. Furthermore, there are no available data examining the ergogenic effect of inhaling a single bolus of the upper daily limit of 1600 µg or the impact on urine concentration of the short-acting β2-agonist and its relationship with the WADA code. Meanwhile, caffeine and theobromine have been regarded as bronchodilators and whilst the potential ergogenic effects of caffeine have led to its WADA monitored status no such information exists for theobromine. Study 1 investigated the ergogenic effect of 800 µg and 1600 µg of salbutamol in a randomised, single-blind and cross-over design on 5-km running time-trial performance in non-asthmatic endurance athletes (n = 7). The study revealed no significant improvement in performance after the inhalation of either doses of salbutamol (t = 1683.29 ± 179.74 sec for 800 µg and t = 1683.57 ± 190.69 sec for 1600 µg) compared with placebo condition (t = 1714.71 ± 186.22 sec). Study 2 employed a simulated football protocol following the inhalation of 800 µg and 1600 µg of salbutamol in a randomised, single-blind placebo controlled trial in male (n = 7) and female (n = 6) football players. Results demonstrated there is an improvement of inhaled salbutamol on performance. Whilst the average urine salbutamol concentrations did not breach the WADA urinary threshold (1000 ng·mL-1), five individuals, two male and three female, recorded urine drug concentrations that exceeded the threshold. Study 3 examined the urine concentration of salbutamol following passive body mass loss of 2% or 5% following the inhalation of 800 µg and 1600 µg of salbutamol across ethnicity and gender (n = 32). The study demonstrated that following the inhalation of 1600µg it is possible to present urine salbutamol concentrations above the current WADA upper limit that imposes a urinary drug threshold of 1000 ng·mL-1. Study 4 explored the ergogenic effect of caffeine and theobromine on non-asthmatic athletes during a 3-km time trial (n = 10). The findings suggest that both caffeine and theobromine resulted in an improved time-trial performance (t = 1168.7 ± 78.12 sec and t = 1176.5 ± 75.15 sec, respectively) compared with placebo condition (t = 1260.6 ± 110.65 sec), while caffeine resulted in a larger and more rapid enhancement compared to theobromine. Overall, salbutamol, the intake of which is restricted by WADA, did not have an ergogenic effect on athletes, while on the other hand, caffeine and theobromine, the usage of which are not controlled at all in sports competitions, had a performance enhancing effect on athletes, according to our results. Furthermore, although the inhalation of salbutamol did not improve the overall performance, athletes inhaling these substances might record urine concentration exceeding the WADA threshold, resulting in an adverse analytical finding (AAF).